Obstructive sleep apnea syndrome increases serum angiotensin II and incidence of non-dipping circadian blood pressure in patients with essential hypertension

Abstract

Obstructive sleep apnea syndrome (OSAS) is closely associated with hypertension. Activity of angiotensin II (Ang II) and non‐dipping nocturnal blood pressure (BP) variability are implicated in hypertension‐related target organ damage. We examined the correlation between OSAS with serum Ang II levels and evaluated the risk of non‐dipping BP variability in 180 patients with essential hypertension (EHT). Eligible patients were divided into three subgroups based on their apnea–hypopnea index (AHI) evaluated by polysomnography. EHT alone, EHT with mild OSAS, and EHT with moderate/severe OSAS. Ambulatory BP monitoring was used to calculate mean BP over 24 h, as well as diurnal and nocturnal BP variability. Serum Ang II was determined with enzyme‐linked immunosorbent assay. EHT patients with OSAS had significantly higher systolic BP calculated either over 24 h, or by diurnal or nocturnal monitoring (P < 0.05). More EHT patients with OSAS showed non‐dipping BP profiles than did EHT patients alone (P < 0.05). The number of patients with non‐dipping BP increased with increasing OSAS severity. Surgical treatment alleviated OSAS and reduced AHI (P < 0.05). Preoperative serum Ang II in EHT patients with OSAS was significantly higher than that in those without OSAS (P < 0.05), and showed a rising trend with OSAS severity (P < 0.05). Postoperative serum Ang II, BP and the incidence of non‐dipping BP were reduced by surgery to levels lower than preoperative values in patients with OSAS. We therefore conclude that OSAS leads to increased serum Ang II and increased risk of non‐dipping BP in patients with EHT.

The Prevalence and Clinical Features of Hypertension in Patients With Obstructive Sleep Apnea Hypopnea Syndrome and Related Nursing Strategies

“…The prorenin-and angiotensin-converting enzymes show a CR as well. It has been shown that OSAHS may disturb the RAAS through chronic recurrent hypoxia and hypercapnia, which frequently occurs at night and results in increased serum Ang II and endothelin levels in essential hypertensive patients (Belaidi et al, 2009;Wang et al, 2012). OSAHS leads to increased serum Ang II and increased risk of nondipping BP in patients with essential hypertension.…”

The treatment of mild OSA with CPAP or mandibular advancement device and the effect on blood pressure and endothelial function after one year of treatment

“…[13][14][15]17 A study using upper airway surgery in a sample of patients with hypertension associated with mild OSA showed improvement in mean 24-hour systolic BP, daytime diastolic blood pressure, nocturnal systolic blood pressure, and dipping pattern compared to their pretreatment condition. 16 A prospective observational cohort study, which did a subanalysis with a mild OSA subgroup, found no differences between patients using CPAP and those who declined CPAP or did not adhere to treatment in relation to incidence of hypertension. 18 There has been some discussion of whether mild OSA should be treated.…”

“…Randomized clinical trials are still needed of CPAP and MAD in patients with mild OSA exclusively and including comorbidities. Previous studies evaluating the effects of mild OSA on cardiovascular outcomes were mainly retrospective, 9 had a small sample size, 10 included other OSA severity levels, [11][12][13] used other treatments as interventions, [14][15][16][17] or were population studies. 18 Considering the relative lack of clinical research on the use of CPAP or MAD in the treatment of mild OSA, associated or not with symptoms and comorbidities, we hypothesized that treatment with CPAP or MAD would improve blood pressure and endothelial function compared with no treatment after 1 year of follow-up.…”

Prevalence of hypertension and circadian blood pressure variations in patients with obstructive sleep apnoea–hypopnoea syndrome

“…17 It has been reported that OSAHS may disturb the RAAS due to the chronic recurrent hypoxia and hypercapnia that frequently occur at night, resulting in increased serum angiotensin II and endothelin levels in patients with essential hypertension. 12,18 These patients are more likely to develop a non-dipping BP pattern and consequently are at higher risk of cardiovascular events, end-organ damage and mortality, independent of the BP load. 19 Similar to the results of the present study, Stergiou et al 19 reported that an increase in AHI at night was associated with an absence of nocturnal dipping and a significant increase in urinary catecholamine levels.…”

“…For history of snoring: 2 ¼ 458.27, v ¼ 3, P 0.001 between groups. For prevalence of hypertension: 2 ¼ 159 18,. v ¼ 3, P < 0.001 between groups.…”